The most recent outbreak of equine herpesvirus myeloencephalopathy (EHM) has finally subsided. The report, “Equine Herpesvirus Myeloencephalopathy: Mitigation Experiences, Lessons Learned, and Future Needs” (see PDF) is based on interviews with 18 veterinarians or state equine program managers who worked to control recent outbreaks of EHM. With warm weather comes the increased risk of snakebite. For this reason, some experts believe that EHM should be classified as a newly emerging infectious disease. VDACS officials advise that strict biosecurity is the most effective way to minimize the risk of spreading the virus. People can spread the disease, too, if their hands, clothing, shoes or vehicles are contaminated, so wear coveralls, boot covers or use disinfectant baths if feasible. The potential for EHV-1 to cause Equine Herpesvirus Myeloencephalopathy is influenced by a number of factors and case reports vary from involving a single horse to very large numbers of cases.
All were infected with equine herpesvirus-1 of DNA polymerase D752 genotype. Conclusion and Clinical Importance: These results suggest that nasal shedding and viremia of EHV-1 in hospitalized critically ill horses with acute abdominal disorder is extremely rare. Implementation of additional biosecurity protocols to limit aerosol spread of EHV-1 among horses with acute abdominal disease and other hospitalized horses is not necessary. Equid herpesvirus-1 (EHV-1) is the etiologic agent of 3 syndromes: respiratory disease (rhinopneumonitis), reproductive disease (abortion and neonatal illness), and neurologic disease (equine herpesvirus myeloencephalopathy [EHM]).1 Occurrence of the neurologic form of EHV-1 appears to be increasing.1,2 Cancellation of equine sporting events to limit the spread of EHV-1 and the high mortality rates associated with the neurologic and reproductive syndromes have resulted in substantial economic impact to the equine industry. With increased concern about transmission of EHV-1 and subsequent development of EHM, many equine hospitals have modified biosecurity policies to include isolation of horses presenting with neurologic signs consistent with EHV-1 infection. Horses with critical illnesses typically are under substantial stress, and increased serum cortisol and catecholamine concentrations have been documented in such horses.15 In addition, many of these patients have leukopenia and altered immune status as a result of their primary disease.16,17 No information exists on the effect of acute critical illness on potential EHV-1 reactivation and shedding, although reactivation has been reported in horses with terminal illness. (Posterior incoordination, weakness, recumbency with inability to rise, and/or bladder atony are most commonly seen in EHM cases.) Confirmed EHM case: A suspect EHM case with laboratory confirmation of EHV-1 infection.
VDACS began an epidemiological investigation on February 13 and will continue to monitor the situation. In the case of EHV-1 abortions, the fetal tissues and fluids contain high concentrations of virus; infected foals and mares also shed virus via the respiratory route. Viral activation was assumed when both mRNA and DNA for the gB gene was detected. A difference in gene expression after activation of the UPR in two equine cell types was found. This information will help to better understand whether acute abdominal disease is a strong trigger of reactivation. One hundred and twenty-four horses met the inclusion criteria. There were 89 surgical colic and 35 colitis cases.
Age ranged from 6 months to 28 years with a mean age of 10 years. Fourteen horses (11%) were ≤2 years of age at the time of illness. Bibliography Allen, G., Kydd, J., Slater, J. There were 34 Quarterhorses, 24 Thoroughbreds, 18 Arabians, 11 Warmbloods, 9 Draft horses, 4 Appaloosa and Morgan horses, 3 Tennessee Walking Horses and Friesians, 2 American Paint Horses, Ponies, Standardbreds, and American Miniature Horses, and 1 Paso Fino, Donkey, Mustang, and mixed-breed horse. One hundred and nine horses (88%) survived to discharge. Seven horses with colic and 8 horses with colitis were euthanized or died. Only by working together can we prevent a debilitating outbreak.
In all cases, blood and nasal secretions tested negative for the presence of the EHV-1 gB and the ORF 30 gene. All samples passed quality control after precipitation and preamplification based on established eGAPDH values (cycle threshold range 9–13) confirming the presence of DNA and mRNA. MLN tissue was collected from 9 horses enrolled in the study and from 26 Michigan horses euthanized for reasons excluding respiratory disease, neurologic disease, or reproductive disease. Of these 26 horses, there were 15 geldings, 10 mares, and 1 stallion. Age ranged from 1 to 34 years with a mean of 19 years. Lymph node tissue from all 35 horses tested negative for the EHV-1 gB and the ORF 30 genes and positive for the eGAPDH gene. Many of these older horses remain actively involved in equestrian sport competitions, are still being bred, or serve as companion animals.
The negative results are unlikely to be because of the lack of sensitivity of the methodology utilized because the method has been shown to be capable of detecting 1 copy number of the target gene per tissue sample processed.11 The negative results could be due in part to a low level of latency within the population examined or because acute abdominal disease does not trigger reactivation of latent EHV-1. MLN samples were collected from enrolled patients to enable determination of the EHV-1 latency rate within the population studied. Unfortunately, although many clients were willing to enroll their horses in this study they were unwilling to allow MLN biopsy collection. Consequently, we were only able to collect MLN tissues from 9 horses and were unable to determine accurately if the lack of detectable virus within this population was because of a low reactivation rate or a low latency rate. In an effort to address this problem, we collected MLN tissues from an additional 26 Michigan horses presented for post mortem evaluation at the Diagnostic Center for Population and Animal Health at MSU. Although these horses were not members of the study population, they represented one of the larger groups (Michigan horses) from which the study population was taken. Similar to the study population, all MLN were negative for the presence of EHV-1 DNA, supporting the conclusion that MLN latency rates are low in this population of horses.
However, in a recent study by Pusterla et al18 the authors reported a higher latency rate in the trigeminal ganglia compared with the MLN. In this report, the authors detected latent virus in 12.4% of the trigeminal ganglia sampled and only 3.3% of the MLN samples, suggesting that the trigeminal ganglia may be a more appropriate tissue to sample when determining latency using the same methodology as used in this report. These samples were collected over the same time frame as our study and therefore are indicative of the latency rate of horses in California from which our study population was obtained. Both the results from the study by Pusterla and colleagues and those of our study are in contrast to those reported by Allen and colleagues in which they reported a latency rate of 54% in the MLN from 132 Thoroughbred broodmares.10,18 Although the methodology used by Allen and colleagues differed from that used in our study, both methods have been shown to be capable of detecting as few as 1 copy of a target sequence per sample.10,11 Trigeminal ganglia were not examined in the study by Allen et al.10 In summary, the overall latency rate of EHV-1 in adult horses and the ideal sampling site to detect latency are unknown. Therefore, we cannot determine whether a low latency rate was a factor in the absence of reactivation in this population. The difference in MLN latency rates found in Allen’s, Pusterla’s, and our data may be because of the difference in populations and management practices associated with large breeding farms as opposed to other husbandry settings. In the paper by Allen et al10 the population examined was principally broodmares whereas most of the horses in our study were performance animals.
Broodmares tend to be housed in groups with other mares and foals in breeding operations. This housing situation may increase the spread of EHV-1 between mares and foals resulting in a greater incidence of infection and subsequent latency than seen in other populations.19 Although several of the horses included in this study were broodmares, or housed with broodmares, the size of these operations generally was quite small and the diversity of horses found on the premises varied a great deal. Although the authors recognize that the MLN latency rates detected in the small sample of MSU horses euthanized for other reasons (0%) and the larger group of UC Davis horses published previously (3.3%) does not exactly reflect the latency rate within our study population, we believe this information is valuable in that it provides additional information regarding latency rates in the larger populations sampled. Given the substantial differences between the MLN latency rates and those published previously, we feel this information is important when assessing the results of our study. It is possible that reactivation may have occurred between sampling times and, as a result, been undetected. Analysis of serum titers may have helped detect these cases because serum titers will increase after infection and viremia. 1955.
More information on the duration of viremia and shedding after reactivation is needed to better determine the effect of sampling frequency on these results. In conclusion, it appears that the risk of EHV-1 shedding and viremia in hospitalized, critically ill horses presenting with acute abdominal disease is extremely low. In this population of horses, biosecurity protocols currently focus on barrier protocols to limit spread of pathogens in feces. The results of this study suggest that additional biosecurity measures for prevention of aerosol spread of EHV-1 do not appear to be necessary for the acute abdominal patient. The results from this and other studies suggest that frequency of latency of EHV-1 in different horse populations may vary considerably. In addition, latency rates and detection may vary depending on the site selected. Consequently, we cannot determine whether the lack of reactivation and shedding is because acute abdominal disease is not a clinically important trigger of reactivation or because few horses in this population carry latent virus.
Additional information on latency rates within the trigeminal ganglia would be needed to more accurately assess the results of this study. The results of this study suggest that although performing nasal swabs and peripheral blood PCR for EHV-1 in a febrile postoperative patient would be thorough, it would be unlikely to yield a positive result. Given the high latency rates reported for broodmares in the southeastern United States, the authors caution against applying this data throughout the country. Basic research is often conducted in laboratories away from horse farms and racetracks.